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Updated: Feb 19, 2026
Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus
Published on: October 7, 2011
The regulatory role of protein phosphorylation in human gammaherpesvirus associated cancers
Yuyan Wang1, Shuvomoy Banerjee2, Ling Ding1
1MOH & MOE Key Laboratory of Medical Molecular Virology, School of Basic Medical Sciences, Shanghai Medical College of Fudan University, Shanghai, 200032, China.
Abstract:
Activation of specific sets of protein kinases by intracellular signal molecules has become more and more apparent in the past decade. Phosphorylation, one of key posttranslational modification events, is activated by kinase or regulatory protein and is vital for controlling many physiological functions of eukaryotic cells such as cell proliferation, differentiation, malignant transformation, and signal transduction mediated by external stimuli. Moreovers, the reversible modification of phosphorylation and dephosphorylation can result in different features of the target substrate molecules including DNA binding, protein-protein interaction, subcellular location and enzymatic activity, and is often hijacked by viral infection. Epstein-Barr virus (EBV) and Kaposi's sarcomaassociated herpesvirus (KSHV), two human oncogenic gamma-herpesviruses, are shown to tightly associate with many malignancies. In this review, we summarize the recent progresses on understanding of molecular properties and regulatory modes of cellular and viral proteins phosphorylation influenced by these two tumor viruses, and highlight the potential therapeutic targets and strategies against their related cancers.
Insights
Protein phosphorylation, a key cellular process, is manipulated by Epstein-Barr virus (EBV) and Kaposi
Area of Science:
- Molecular Biology
- Virology
- Oncology
Background:
- Protein kinases regulate crucial eukaryotic cell functions through phosphorylation.
- Phosphorylation is a vital posttranslational modification controlling cell proliferation, differentiation, and signal transduction.
- Viral infections, including Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV), hijack cellular phosphorylation pathways.
Purpose of the Study:
- To review recent advancements in understanding how EBV and KSHV influence cellular and viral protein phosphorylation.
- To explore the molecular properties and regulatory mechanisms of phosphorylation in the context of these oncogenic gamma-herpesviruses.
- To identify potential therapeutic targets and strategies for cancers associated with EBV and KSHV.
Main Methods:
- Literature review of recent scientific publications.
- Analysis of molecular properties and regulatory modes of protein phosphorylation.
- Focus on cellular and viral proteins affected by EBV and KSHV.
Main Results:
- EBV and KSHV, human oncogenic gamma-herpesviruses, are strongly linked to various malignancies.
- These viruses intricately modulate host cell phosphorylation processes.
- Understanding these viral-host interactions reveals insights into cancer development.
Conclusions:
- EBV and KSHV significantly impact cellular phosphorylation, contributing to oncogenesis.
- Targeting these virus-host phosphorylation interactions offers promising therapeutic strategies.
- Further research into these mechanisms can lead to novel anti-cancer treatments.
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